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Special Issue "Vascular Endothelial Growth Factor"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (31 March 2018).

Special Issue Editor

Guest Editor
Prof. Kurt Ballmer-Hofer

Biomolecular Research, Paul Scherrer Institute, 5232-Villigen, Switzerland; and Biocenter of the University of Basel, 4056-Basel, Switzerland
Website | E-Mail
Interests: VEGF structure and function in angiogenesis; transmembrane signaling by receptor tyrosine kinases

Special Issue Information

Dear Colleagues,

A Special Issue on Vascular Endothelial Growth Factor, VEGF, is being prepared for the journal IJMS. VEGF was originally described as Vascular Permeability Factor, VPF, released by tumor tissue and later found to be the major driver of blood and lymphatic vessel development in mammals. VEGFs are derived from primordial molecules shaping the open vascular system of insects and comprise a family of four members. Additionally, functionally and structurally highly related homologues were found in pox viruses and snake venoms. The four VEGF genes in mammals give rise to a large number of functionally distinct protein isoforms that combinatorially activate three type V receptor tyrosine kinases. The dissection of the complexity of VEGF signaling is the focus of intense research and understanding VEGF signaling at the molecular level has great potential for future medical applications.

Altered functionality and expression of VEGFs and their receptors are the cause of severe human pathologies, such as retinopathies of the eye, atherosclerosis or the promotion and dissemination of cancer. Novel and more specific drugs must be developed for broad and successful application in the clinic in the future.

Prof. Kurt Ballmer-Hofer
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • angiogenesis
  • receptor tyrosine kinase
  • signaling
  • vascular endothelial growth factor

Published Papers (12 papers)

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Editorial

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Open AccessEditorial
Vascular Endothelial Growth Factor, from Basic Research to Clinical Applications
Int. J. Mol. Sci. 2018, 19(12), 3750; https://doi.org/10.3390/ijms19123750
Received: 7 November 2018 / Revised: 20 November 2018 / Accepted: 23 November 2018 / Published: 26 November 2018
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Abstract
Judah Folkman’s landmark discovery in the 1970s showing that tumors, growing beyond a few millimeters in diameter, depend on de novo vascularization triggered by specific growth factors released by tumor cells encountering hypoxia [...] Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor)

Research

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Open AccessArticle
Oxygen-Induced Retinopathy from Recurrent Intermittent Hypoxia Is Not Dependent on Resolution with Room Air or Oxygen, in Neonatal Rats
Int. J. Mol. Sci. 2018, 19(5), 1337; https://doi.org/10.3390/ijms19051337
Received: 6 April 2018 / Revised: 26 April 2018 / Accepted: 27 April 2018 / Published: 1 May 2018
Cited by 2 | PDF Full-text (2431 KB) | HTML Full-text | XML Full-text
Abstract
Preterm infants often experience intermittent hypoxia (IH) with resolution in room air (RA) or hyperoxia (Hx) between events. Hypoxia is a major inducer of vascular endothelial growth factor, which plays a key role in normal and aberrant retinal angiogenesis. This study tested the [...] Read more.
Preterm infants often experience intermittent hypoxia (IH) with resolution in room air (RA) or hyperoxia (Hx) between events. Hypoxia is a major inducer of vascular endothelial growth factor, which plays a key role in normal and aberrant retinal angiogenesis. This study tested the hypothesis that neonatal IH which resolved with RA is less injurious to the immature retina than IH resolved by Hx between events. Newborn rats were exposed to: (1) Hx (50% O2) with brief hypoxia (12% O2); (2) RA with 12% O2; (3) Hx with RA; (4) Hx only; or (5) RA only, from P0 to P14. Pups were examined at P14 or placed in RA until P21. Retinal vascular and astrocyte integrity; retinal layer thickness; ocular and systemic biomarkers of angiogenesis; and somatic growth were determined at P14 and P21. All IH paradigms resulted in significant retinal vascular defects, disturbances in retinal astrocyte template, retinal thickening, and photoreceptor damage concurrent with elevations in angiogenesis biomarkers. These data suggest that the susceptibility of the immature retina to changes in oxygen render no differences in the outcomes between RA or O2 resolution. Interventions and initiatives to curtail O2 variations should remain a high priority to prevent severe retinopathy. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor)
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Open AccessArticle
ScFvs as Allosteric Inhibitors of VEGFR-2: Novel Tools to Harness VEGF Signaling
Int. J. Mol. Sci. 2018, 19(5), 1334; https://doi.org/10.3390/ijms19051334
Received: 30 March 2018 / Revised: 23 April 2018 / Accepted: 23 April 2018 / Published: 1 May 2018
Cited by 1 | PDF Full-text (2714 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Vascular Endothelial Growth Factor Receptor 2 (VEGFR-2) is the main mediator of angiogenic signaling in endothelial cells and a primary responder to VEGF. VEGF dependent VEGFR-2 activation regulates endothelial cell migration and proliferation, as well as vessel permeability. VEGF is presented as an [...] Read more.
Vascular Endothelial Growth Factor Receptor 2 (VEGFR-2) is the main mediator of angiogenic signaling in endothelial cells and a primary responder to VEGF. VEGF dependent VEGFR-2 activation regulates endothelial cell migration and proliferation, as well as vessel permeability. VEGF is presented as an antiparallel homodimer, and its binding to VEGFR-2 brings two receptors in close proximity. Downstream signaling is triggered by receptor dimerization, kinase activation, and receptor internalization. Our aim was to further investigate allosteric inhibition using binders targeting extracellular subdomains 4–7 of VEGFR-2 as an alternative to existing anti-angiogenic therapies, which rely on neutralizing VEGF or blocking of the ligand-binding site on the receptor. We applied phage display technology to produce single chain antibody fragments (scFvs) targeting VEGFR-2. Selected antibody fragments were characterized using biophysical and biological assays. We characterized several antibody fragments, which exert their inhibitory effect of VEGFR-2 independent of ligand binding. These reagents led to rapid clearance of VEGFR-2 from the cell surface without kinase activation, followed by an increase in intracellular receptor-positive vesicles, suggesting receptor internalization. Our highly specific VEGFR-2 binders thus represent novel tools for anti-angiogenic therapy and diagnostic applications. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor)
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Review

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Open AccessReview
The Use of Vascular Endothelial Growth Factor Inhibitors and Complementary Treatment Options in Polypoidal Choroidal Vasculopathy: A Subtype of Neovascular Age-Related Macular Degeneration
Int. J. Mol. Sci. 2018, 19(9), 2611; https://doi.org/10.3390/ijms19092611
Received: 13 July 2018 / Revised: 17 August 2018 / Accepted: 27 August 2018 / Published: 3 September 2018
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Abstract
Polypoidal choroidal vasculopathy (PCV) is a subtype of neovascular age-related macular degeneration (AMD; nAMD) which occurs more commonly in Asian populations as compared to Caucasians. PCV and nAMD share pathological mechanisms, including pathological expression of vascular endothelial growth factor (VEGF). The advent of [...] Read more.
Polypoidal choroidal vasculopathy (PCV) is a subtype of neovascular age-related macular degeneration (AMD; nAMD) which occurs more commonly in Asian populations as compared to Caucasians. PCV and nAMD share pathological mechanisms, including pathological expression of vascular endothelial growth factor (VEGF). The advent of anti-vascular endothelial growth factor (VEGF) revolutionized the treatment of nAMD. Despite being a subtype of nAMD, PCV responds less well to VEGF inhibitors; thus, photodynamic therapy (PDT) in combination with anti-VEGF treatment may be considered. This review aims to summarize the current evidence for the treatment of PCV, especially whether VEGF inhibitors should be used alone or in combination with PDT. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor)
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Open AccessReview
VEGF Upregulation in Viral Infections and Its Possible Therapeutic Implications
Int. J. Mol. Sci. 2018, 19(6), 1642; https://doi.org/10.3390/ijms19061642
Received: 31 March 2018 / Revised: 28 May 2018 / Accepted: 29 May 2018 / Published: 1 June 2018
Cited by 2 | PDF Full-text (470 KB) | HTML Full-text | XML Full-text
Abstract
Several viruses are recognized as the direct or indirect causative agents of human tumors and other severe human diseases. Vascular endothelial growth factor (VEGF) is identified as a principal proangiogenic factor that enhances the production of new blood vessels from existing vascular network. [...] Read more.
Several viruses are recognized as the direct or indirect causative agents of human tumors and other severe human diseases. Vascular endothelial growth factor (VEGF) is identified as a principal proangiogenic factor that enhances the production of new blood vessels from existing vascular network. Therefore, oncogenic viruses such as Kaposi’s sarcoma herpesvirus (KSHV) and Epstein-Barr virus (EBV) and non-oncogenic viruses such as herpes simplex virus (HSV-1) and dengue virus, which lack their own angiogenic factors, rely on the recruitment of cellular genes for angiogenesis in tumor progression or disease pathogenesis. This review summarizes how human viruses exploit the cellular signaling machinery to upregulate the expression of VEGF and benefit from its physiological functions for their own pathogenesis. Understanding the interplay between viruses and VEGF upregulation will pave the way to design targeted and effective therapeutic approaches for viral oncogenesis and severe diseases. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor)
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Open AccessReview
Polarised VEGFA Signalling at Vascular Blood–Neural Barriers
Int. J. Mol. Sci. 2018, 19(5), 1378; https://doi.org/10.3390/ijms19051378
Received: 18 April 2018 / Revised: 2 May 2018 / Accepted: 3 May 2018 / Published: 5 May 2018
Cited by 1 | PDF Full-text (1666 KB) | HTML Full-text | XML Full-text
Abstract
At blood–neural barriers, endothelial VEGFA signalling is highly polarised, with entirely different responses being triggered by luminal or abluminal stimulation. These recent findings were made in a field which is still in its mechanistic infancy. For a long time, endothelial polarity has intuitively [...] Read more.
At blood–neural barriers, endothelial VEGFA signalling is highly polarised, with entirely different responses being triggered by luminal or abluminal stimulation. These recent findings were made in a field which is still in its mechanistic infancy. For a long time, endothelial polarity has intuitively been presumed, and likened to that of epithelial cells, but rarely demonstrated. In the cerebral and the retinal microvasculature, the uneven distribution of VEGF receptors 1 and 2, with the former predominant on the luminal and the latter on the abluminal face of the endothelium, leads to a completely polarised signalling response to VEGFA. Luminal VEGFA activates VEGFR1 homodimers and AKT, leading to a cytoprotective response, whilst abluminal VEGFA induces vascular leakage via VEGFR2 homodimers and p38. Whilst these findings do not provide a complete picture of VEGFA signalling in the microvasculature—there are still unclear roles for heterodimeric receptor complexes as well as co-receptors—they provide essential insight into the adaptation of vascular systems to environmental cues that are naturally different, depending on whether they are present on the blood or tissue side. Importantly, sided responses are not only restricted to VEGFA, but exist for other important vasoactive agents. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor)
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Open AccessReview
The Janus Face of VEGF in Stroke
Int. J. Mol. Sci. 2018, 19(5), 1362; https://doi.org/10.3390/ijms19051362
Received: 28 March 2018 / Revised: 27 April 2018 / Accepted: 1 May 2018 / Published: 4 May 2018
Cited by 4 | PDF Full-text (1083 KB) | HTML Full-text | XML Full-text
Abstract
The family of vascular endothelial growth factors (VEGFs) are known for their regulation of vascularization. In the brain, VEGFs are important regulators of angiogenesis, neuroprotection and neurogenesis. Dysregulation of VEGFs is involved in a large number of neurodegenerative diseases and acute neurological insults, [...] Read more.
The family of vascular endothelial growth factors (VEGFs) are known for their regulation of vascularization. In the brain, VEGFs are important regulators of angiogenesis, neuroprotection and neurogenesis. Dysregulation of VEGFs is involved in a large number of neurodegenerative diseases and acute neurological insults, including stroke. Stroke is the main cause of acquired disabilities, and normally results from an occlusion of a cerebral artery or a hemorrhage, both leading to focal ischemia. Neurons in the ischemic core rapidly undergo necrosis. Cells in the penumbra are exposed to ischemia, but may be rescued if adequate perfusion is restored in time. The neuroprotective and angiogenic effects of VEGFs would theoretically make VEGFs ideal candidates for drug therapy in stroke. However, contradictory to what one might expect, endogenously upregulated levels of VEGF as well as the administration of exogenous VEGF is detrimental in acute stroke. This is probably due to VEGF-mediated blood–brain-barrier breakdown and vascular leakage, leading to edema and increased intracranial pressure as well as neuroinflammation. The key to understanding this Janus face of VEGF function in stroke may lie in the timing; the harmful effect of VEGFs on vessel integrity is transient, as both VEGF preconditioning and increased VEGF after the acute phase has a neuroprotective effect. The present review discusses the multifaceted action of VEGFs in stroke prevention and therapy. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor)
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Open AccessReview
Positive and Negative Regulation of Angiogenesis by Soluble Vascular Endothelial Growth Factor Receptor-1
Int. J. Mol. Sci. 2018, 19(5), 1306; https://doi.org/10.3390/ijms19051306
Received: 10 April 2018 / Revised: 23 April 2018 / Accepted: 24 April 2018 / Published: 27 April 2018
Cited by 12 | PDF Full-text (15018 KB) | HTML Full-text | XML Full-text
Abstract
Vascular endothelial growth factor receptor (VEGFR)-1 exists in different forms, derived from alternative splicing of the same gene. In addition to the transmembrane form, endothelial cells produce a soluble VEGFR-1 (sVEGFR-1) isoform, whereas non-endothelial cells produce both sVEGFR-1 and a different soluble molecule, [...] Read more.
Vascular endothelial growth factor receptor (VEGFR)-1 exists in different forms, derived from alternative splicing of the same gene. In addition to the transmembrane form, endothelial cells produce a soluble VEGFR-1 (sVEGFR-1) isoform, whereas non-endothelial cells produce both sVEGFR-1 and a different soluble molecule, known as soluble fms-like tyrosine kinase (sFlt)1-14. By binding members of the vascular endothelial growth factor (VEGF) family, the soluble forms reduce the amounts of VEGFs available for the interaction with their transmembrane receptors, thereby negatively regulating VEGFR-mediated signaling. In agreement with this activity, high levels of circulating sVEGFR-1 or sFlt1-14 are associated with different pathological conditions involving vascular dysfunction. Moreover, sVEGFR-1 and sFlt1-14 have an additional role in angiogenesis: they are deposited in the endothelial cell and pericyte extracellular matrix, and interact with cell membrane components. Interaction of sVEGFR-1 with α5β1 integrin on endothelial cell membranes regulates vessel growth, triggering a dynamic, pro-angiogenic phenotype. Interaction of sVEGFR-1/sFlt1-14 with cell membrane glycosphingolipids in lipid rafts controls kidney cell morphology and glomerular barrier functions. These cell–matrix contacts represent attractive novel targets for pharmacological intervention in addition to those addressing interactions between VEGFs and their receptors. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor)
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Open AccessReview
VEGF (Vascular Endothelial Growth Factor) and Fibrotic Lung Disease
Int. J. Mol. Sci. 2018, 19(5), 1269; https://doi.org/10.3390/ijms19051269
Received: 12 March 2018 / Revised: 10 April 2018 / Accepted: 18 April 2018 / Published: 24 April 2018
Cited by 5 | PDF Full-text (975 KB) | HTML Full-text | XML Full-text
Abstract
Interstitial lung disease (ILD) encompasses a group of heterogeneous diseases characterised by varying degrees of aberrant inflammation and fibrosis of the lung parenchyma. This may occur in isolation, such as in idiopathic pulmonary fibrosis (IPF) or as part of a wider disease process [...] Read more.
Interstitial lung disease (ILD) encompasses a group of heterogeneous diseases characterised by varying degrees of aberrant inflammation and fibrosis of the lung parenchyma. This may occur in isolation, such as in idiopathic pulmonary fibrosis (IPF) or as part of a wider disease process affecting multiple organs, such as in systemic sclerosis. Anti-Vascular Endothelial Growth Factor (anti-VEGF) therapy is one component of an existing broad-spectrum therapeutic option in IPF (nintedanib) and may become part of the emerging therapeutic strategy for other ILDs in the future. This article describes our current understanding of VEGF biology in normal lung homeostasis and how changes in its bioavailability may contribute the pathogenesis of ILD. The complexity of VEGF biology is particularly highlighted with an emphasis on the potential non-vascular, non-angiogenic roles for VEGF in the lung, in both health and disease. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor)
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Open AccessReview
Molecular Pharmacology of VEGF-A Isoforms: Binding and Signalling at VEGFR2
Int. J. Mol. Sci. 2018, 19(4), 1264; https://doi.org/10.3390/ijms19041264
Received: 28 March 2018 / Revised: 14 April 2018 / Accepted: 16 April 2018 / Published: 23 April 2018
Cited by 21 | PDF Full-text (3196 KB) | HTML Full-text | XML Full-text
Abstract
Vascular endothelial growth factor-A (VEGF-A) is a key mediator of angiogenesis, signalling via the class IV tyrosine kinase receptor family of VEGF Receptors (VEGFRs). Although VEGF-A ligands bind to both VEGFR1 and VEGFR2, they primarily signal via VEGFR2 leading to endothelial cell proliferation, [...] Read more.
Vascular endothelial growth factor-A (VEGF-A) is a key mediator of angiogenesis, signalling via the class IV tyrosine kinase receptor family of VEGF Receptors (VEGFRs). Although VEGF-A ligands bind to both VEGFR1 and VEGFR2, they primarily signal via VEGFR2 leading to endothelial cell proliferation, survival, migration and vascular permeability. Distinct VEGF-A isoforms result from alternative splicing of the Vegfa gene at exon 8, resulting in VEGFxxxa or VEGFxxxb isoforms. Alternative splicing events at exons 5–7, in addition to recently identified posttranslational read-through events, produce VEGF-A isoforms that differ in their bioavailability and interaction with the co-receptor Neuropilin-1. This review explores the molecular pharmacology of VEGF-A isoforms at VEGFR2 in respect to ligand binding and downstream signalling. To understand how VEGF-A isoforms have distinct signalling despite similar affinities for VEGFR2, this review re-evaluates the typical classification of these isoforms relative to the prototypical, “pro-angiogenic” VEGF165a. We also examine the molecular mechanisms underpinning the regulation of VEGF-A isoform signalling and the importance of interactions with other membrane and extracellular matrix proteins. As approved therapeutics targeting the VEGF-A/VEGFR signalling axis largely lack long-term efficacy, understanding these isoform-specific mechanisms could aid future drug discovery efforts targeting VEGF receptor pharmacology. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor)
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Open AccessReview
Vascular Endothelial Growth Factor-A Exerts Diverse Cellular Effects via Small G Proteins, Rho and Rap
Int. J. Mol. Sci. 2018, 19(4), 1203; https://doi.org/10.3390/ijms19041203
Received: 14 March 2018 / Revised: 3 April 2018 / Accepted: 12 April 2018 / Published: 16 April 2018
Cited by 7 | PDF Full-text (4124 KB) | HTML Full-text | XML Full-text
Abstract
Vascular endothelial growth factors (VEGFs) include five molecules (VEGF-A, -B, -C, -D, and placental growth factor), and have various roles that crucially regulate cellular functions in many kinds of cells and tissues. Intracellular signal transduction induced by VEGFs has been extensively studied and [...] Read more.
Vascular endothelial growth factors (VEGFs) include five molecules (VEGF-A, -B, -C, -D, and placental growth factor), and have various roles that crucially regulate cellular functions in many kinds of cells and tissues. Intracellular signal transduction induced by VEGFs has been extensively studied and is usually initiated by their binding to two classes of transmembrane receptors: receptor tyrosine kinase VEGF receptors (VEGF receptor-1, -2 and -3) and neuropilins (NRP1 and NRP2). In addition to many established results reported by other research groups, we have previously identified small G proteins, especially Ras homologue gene (Rho) and Ras-related protein (Rap), as important mediators of VEGF-A-stimulated signaling in cancer cells as well as endothelial cells. This review article describes the VEGF-A-induced signaling pathways underlying diverse cellular functions, including cell proliferation, migration, and angiogenesis, and the involvement of Rho, Rap, and their related molecules in these pathways. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor)
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Open AccessReview
VEGF Signaling in Neurological Disorders
Int. J. Mol. Sci. 2018, 19(1), 275; https://doi.org/10.3390/ijms19010275
Received: 27 November 2017 / Revised: 6 January 2018 / Accepted: 10 January 2018 / Published: 17 January 2018
Cited by 9 | PDF Full-text (1441 KB) | HTML Full-text | XML Full-text
Abstract
Vascular endothelial growth factor (VEGF) is a potent growth factor playing diverse roles in vasculogenesis and angiogenesis. In the brain, VEGF mediates angiogenesis, neural migration and neuroprotection. As a permeability factor, excessive VEGF disrupts intracellular barriers, increases leakage of the choroid plexus endothelia, [...] Read more.
Vascular endothelial growth factor (VEGF) is a potent growth factor playing diverse roles in vasculogenesis and angiogenesis. In the brain, VEGF mediates angiogenesis, neural migration and neuroprotection. As a permeability factor, excessive VEGF disrupts intracellular barriers, increases leakage of the choroid plexus endothelia, evokes edema, and activates the inflammatory pathway. Recently, we discovered that a heparin binding epidermal growth factor like growth factor (HB-EGF)—a class of EGF receptor (EGFR) family ligands—contributes to the development of hydrocephalus with subarachnoid hemorrhage through activation of VEGF signaling. The objective of this review is to entail a recent update on causes of death due to neurological disorders involving cerebrovascular and age-related neurological conditions and to understand the mechanism by which angiogenesis-dependent pathological events can be treated with VEGF antagonisms. The Global Burden of Disease study indicates that cancer and cardiovascular disease including ischemic and hemorrhagic stroke are two leading causes of death worldwide. The literature suggests that VEGF signaling in ischemic brains highlights the importance of concentration, timing, and alternate route of modulating VEGF signaling pathway. Molecular targets distinguishing two distinct pathways of VEGF signaling may provide novel therapies for the treatment of neurological disorders and for maintaining lower mortality due to these conditions. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor)
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Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
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